M and P Pathway Sensitivities and Their Contribution to Motion Processing in Adolescents with ASD and Adolescents with Siblings with ASD

Background:

Children with Autism Spectrum Disorders (ASD) are known to exhibit deficits in visual motion processing (Dakin and Frith, 2005). Cortical motion processors receive input from sub-cortical magnocellular (M) and parvocellular (P) pathways, so these pathways could play a role in the motion deficit. Infant siblings of individuals with ASD have shown higher relative M versus P pathway sensitivities when compared to control infants (McCleery, Allman, Carver & Dobkins, 2007). This effect observed in siblings is a potential endo-phenotypic marker of ASD, suggesting that ASD may be associated with atypical M versus P functioning early in infancy. Children/adolescents with ASD have shown typical M pathway sensitivities (Bertone et al, 2005, Pellicano et al, 2005), with some evidence for impaired P pathway sensitivities (Davis et al, 2006). However, these studies only compared absolute M and P pathway sensitivities between groups. To date, no study of ASD has compared relative M versus P pathway sensitivities between children/adolescents with ASD and typically-developing (TD) children/adolescents. The extent to which atypicalities in one/both of these pathways could contribute to motion deficits in ASD has also not been investigated.

Objectives:

In this study, relative M versus P functioning in children/adolescents with ASD, as well as the strength of input from these pathways to motion processing were measured. Adolescents with siblings diagnosed with ASD (SIBS) were also tested to explore the existence of an endo-phenotype.

Methods:

Data were collected from 19 participants with ASD, 19 TD participants and 12 SIBS participants, matched on chronological age (mean=180months) and non-verbal IQ (mean=107). For each participant, contrast sensitivity was obtained for moving luminance (light/dark) and isoluminant chromatic (red/green) sinusoidal gratings, in a detection (DET) task, and a direction-of-motion discrimination (MOT) task. Relative M versus P pathway sensitivity was indexed by the log ratio of contrast sensitivity of luminance versus chromatic gratings (L:C) in the DET task. Relative contribution of M and P pathway for motion processing was indexed by the difference in log DET/MOT sensitivity ratios for luminance and chromatic gratings (Diff-Ratio).

Results:

ASD participants exhibited overall lower contrast sensitivity than TD and SIBS participants for the MOT task but not for the DET task (F(2,47)=3.67, p=0.033). ASD participants and TD participants did not differ on L:C ratios. However, SIBS participants showed L:C ratios lower than those of TD and ASD participants (H(2)=6.97, p=0.031), which indicates that the SIBS participants possessed lower relative M versus P pathway sensitivities There were no group differences in Diff-Ratios.

Conclusions:

Impaired performance on the MOT task in the ASD participants confirms previous reports of motion deficits in ASD. Their comparable L:C ratios and Diff-Ratios with TD participants suggest that the motion deficit is not driven by atypical relative M versus P functioning, or atypical relative strength of M and P pathway input to motion processing. Finally, the lower L:C ratios in SIBS participants, which is in the direction opposite to that reported in infant SIBS (McCleery et al., 2007), may reflect a compensatory developmental mechanism in individuals who have a genetic pre-disposition for ASD.